Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Extracellular signal-regulated mitogen-activated protein kinase inhibitors decrease amphetamine-induced behavior and

X Shi1, J F McGinty

  • 1Department of Neurosciences, Medical University of South Carolina, 173 Ashley Avenue, BSB 403, Charleston, SC 29425, USA.

Neuroscience
|February 7, 2006
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effects of brain-derived neurotrophic factor on dopaminergic function and motor behavior during aging.

Genes, brain, and behavior·2010
Same author

Context-driven cocaine-seeking in abstinent rats increases activity-regulated gene expression in the basolateral amygdala and dorsal hippocampus differentially following short and long periods of abstinence.

Neuroscience·2010
Same author

Glutamate-dopamine interactions mediate the effects of psychostimulant drugs.

Addiction biology·2010
Same author

Amphetamine up-regulates activator of G-protein signaling 1 mRNA and protein levels in rat frontal cortex: the role of dopamine and glucocorticoid receptors.

Neuroscience·2010
Same author

Intrahippocampal NMDA Administration Alters Fos, Fos-Related Antigens, and Opioid Peptide Immunoreactivity and mRNA in Rats.

Molecular and cellular neurosciences·2009
Same author

Amphetamine-induced locomotion and gene expression are altered in BDNF heterozygous mice.

Genes, brain, and behavior·2008

Inhibiting the extracellular-regulated kinase (ERK) pathway reduces amphetamine-induced hyperactivity and changes in neuropeptide gene expression in rat brains. This suggests ERK signaling is crucial for amphetamine

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Amphetamine administration causes significant behavioral changes and alters gene expression in the rat striatum.
  • The extracellular-regulated kinase (ERK) signaling pathway is implicated in various neuronal functions and responses to drugs.

Purpose of the Study:

  • To investigate if inhibiting the ERK signaling pathway affects acute amphetamine-induced behavioral activity and neuropeptide gene expression in the rat striatum.
  • To elucidate the role of ERK activation in the neurobiological effects of amphetamine.

Main Methods:

  • Western blotting was used to assess ERK phosphorylation levels post-amphetamine administration.
  • Systemic administration of SL327 (an ERK kinase inhibitor) and intra-striatal infusion of U0126 were employed to inhibit ERK signaling.

Related Experiment Videos

  • Behavioral activity (vertical and horizontal) was monitored, and quantitative in situ hybridization histochemistry was used to measure neuropeptide mRNA levels (preproenkephalin and preprodynorphin).

    • Main Results:

    • Acute amphetamine significantly increased ERK1/2 phosphorylation in the rat striatum.
    • Inhibition of ERK signaling by SL327 or U0126 markedly reduced amphetamine-induced hyperlocomotor activity.
    • SL327 and U0126 blocked amphetamine-induced increases in preproenkephalin and preprodynorphin mRNA levels in the striatum.

    Conclusions:

    • Activation of the ERK signaling cascade is a key mechanism underlying the behavioral effects of acute amphetamine.
    • The ERK pathway mediates amphetamine-induced changes in striatal neuropeptide gene expression.
    • Targeting the ERK pathway may offer therapeutic strategies for managing amphetamine-induced behavioral disturbances.